Serotonin type II receptor activation facilitates synaptic plasticity via N-methyl-D-aspartate-mediated mechanism in the rat basolateral amygdala
Serotonin type II receptor activation facilitates synaptic plasticity via N-methyl-D-aspartate-mediated mechanism in the rat basolateral amygdala
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DOI：
10.1016/s0306-4522(03)00076-9
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发表时间：
2003-01-01
期刊：
影响因子：
3.3
通讯作者：
Li, H
中科院分区：
文献类型：
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作者：
Chen, A;Hough, CJ;Li, H
利用细胞内、场电位和Fura-2荧光图像记录大鼠杏仁核切片，探讨了5-羟色胺II型（5-羟色胺II型（5-HT2））受体刺激对突触可塑性的调节。5HT(2)受体激动剂1-(2,5)-二甲氧基-4- lodopen -2-氨基丙烷（DOI）的大量应用将θ -爆发刺激（TBS）突触可塑性从短期增强转变为长期增强。DOI增强n -甲基- d -天冬氨酸（NMDA）受体介导的电位和钙内流，而不影响神经元的静息膜电位或输入阻抗。相比之下，α -氨基-3-羟基-5-甲基-4-异恶唑丙酸酯(AMPA)/盐酸盐受体介导的兴奋性突触反应不受DOI的影响。DOI的促进作用被5-HT2受体拮抗剂酮色林和5- ht2c受体选择性拮抗剂RS102221阻断。这些结果表明，5- ht2受体的激活增强了基底外侧杏仁核（BLA）中NMDA受体介导的突触功能。(C)由Elsevier Science Ltd代表IBRO出版。
The modulation of synaptic plasticity by serotonin type II (5-hydroxytryptamine type II (5-HT2))-receptor stimulation was explored using intracellular, field potential and Fura-2 fluorescence image recordings in a rat amygdala slice preparation. Bath application of 5HT(2) receptor agonist 1-(2,5)-dimethoxy-4-lodophen-2-aminopropane (DOI) transformed theta-burst-stimulated (TBS) synaptic plasticity from short-term potentiation to long-term potentiation. DOI enhanced N-methyl-D-aspartate (NMDA) receptor-mediated potentials and calcium influx without affecting the resting membrane potential or input resistance of the neurons. In contrast, alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA)/kainate receptor-mediated excitatory synaptic responses were unaffected by DOI. The facilitating effects of DOI were blocked by the 5-HT2 receptor antagonist, ketanserin, and by the 5-HT2C-receptor selective antagonist, RS102221. These results indicate that 5-HT2-receptor activation enhances NMDA receptor-mediated synaptic function in the basolateral amygdala (BLA). (C) Published by Elsevier Science Ltd on behalf of IBRO.